FIGURE 2: The lesion partially calcified without significant postcontrast enhancement in the left striatocapsular region. The reduction of the edema component, which does not currently extend to the temporal lobe,… Click to show full abstract
FIGURE 2: The lesion partially calcified without significant postcontrast enhancement in the left striatocapsular region. The reduction of the edema component, which does not currently extend to the temporal lobe, is more evident in T2 and FLAIR. Reduction of the mass effect on the ventricular system, with the incipient deviation of the pellucid septum to the right persisting. A 75-year-old male was admitted to the emergency department with right-sided weakness for 3 weeks and fever (38 °C). His medical history included rheumatoid arthritis treated with adalimumab and methotrexate. Neurological examination revealed right central facial palsy and right brachial hemiparesis with a motor strength of 3/5 in the right extremities. Laboratory tests did not reveal alterations. Serological tests showed positivity for toxoplasma immunoglobulin G (>300 IU/mL) with immunoglobulin M negativity. Brain magnetic resonance imaging (MRI) revealed a centered lesion without significant postcontrast enhancement (Figure 1). Even though the radiological findings were not fully conclusive, they pointed to an infectious cause. A lumbar puncture was performed and the polymerase chain reaction (PCR) for Toxoplasma gondii in the cerebrospinal fluid was positive. Despite the atypical imaging appearance, the analysis of the entire clinical picture with PCR for T. gondii positivity suggested the diagnosis of cerebral toxoplasmosis. The patient started therapy with pyrimethamine, sulfadiazine, and folinic acid. At discharge, he recovered completely from his neurological deficits. After finishing the treatment, MRI showed improvement in edema with a practically calcified lesion (Figure 2).
               
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